Muscle Response to IL-6 Defective in Type 2 DiabetesLast Updated: October 25, 2012. Skeletal muscle cells from people with type 2 diabetes have defects in glucose metabolism but have normal lipid metabolism after treatment with interleukin-6, according to a study published online Oct. 18 in Diabetes.
THURSDAY, Oct. 25 (HealthDay News) -- Skeletal muscle cells from people with type 2 diabetes have defects in glucose metabolism but have normal lipid metabolism after treatment with interleukin-6 (IL-6), according to a study published online Oct. 18 in Diabetes.
Noting that IL-6 both enhances and inhibits the action of insulin, Lake Q. Jiang, from the Karolinska Institutet in Stockholm, and colleagues investigated how IL-6 affected glucose and lipid metabolism in cultured myotubes from people with normal glucose tolerance and from people with type 2 diabetes.
The researchers found that, in myotubes from people with normal glucose tolerance, IL-6 treatment increased glycogen synthesis, glucose uptake, and phosphorylation of signal transducer and activator of transcription 3 (STAT3). In contrast, IL-6 had no effect on glucose metabolism or STAT3 signaling but did increase expression of suppressor of cytokine signaling 3 in people with type 2 diabetes. IL-6 increased fatty acid oxidation in myotubes from both groups. Cultured myotubes from both groups had similar levels of IL-6, IL-6 receptor, and glycoprotein 130, as well as similar IL-6 secretion.
"In summary, skeletal muscle cells from type 2 diabetic patients display selective IL-6 resistance for glucose rather than lipid metabolism," Jiang and colleagues conclude. "IL-6 appears to play a differential role in regulating metabolism in type 2 diabetic patients compared with normal glucose-tolerant subjects."
The study was funded in part by the Novo Nordisk Research Foundation.
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